Fumigaclavine C, an fungal metabolite, improves experimental colitis in mice via downregulating Th1 cytokine production and matrix metalloproteinase activity.

Abstract	In the present paper, the effect of Fumigaclavine C, a fungal metabolite, on experimental colitis was examined. Fumigaclavine C, when administered intraperitoneally once a day, significantly reduced the weight loss and mortality rate of mice with experimental colitis induced by intrarectally injection of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). This compound also markedly alleviated the macroscopic and microscopic appearances of colitis. Furthermore, Fumigaclavine C, given both in vivo and in vitro, showed a marked inhibition on the expression of several inflammatory cytokines, including IL-1beta, IL-2, IL-12alpha, IFN-gamma, TNF-alpha as well as MMP-9 in sacral lymph node cells, colonic patch lymphocytes and colitis tissues from the TNBS colitis mice. Meanwhile, the compound caused a dose-dependent reduction in IL-2 and IFN-gamma from the lymphocytes at the protein level and MMP-9 activity. These results suggest that Fumigaclavine C may alleviate experimental colitis mainly via down-regulating the production of Th1 cytokines and the activity of matrix metalloproteinase.
Authors	Xue-Feng Wu, Ming-Jian Fei, Ren-Geng Shu, Ren-Xiang Tan, Qiang Xu
Journal	International immunopharmacology (Int Immunopharmacol) Vol. 5 Issue 10 Pg. 1543-53 (Sep 2005) ISSN: 1567-5769 [Print] Netherlands
PMID	16023606 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Cytokines Ergot Alkaloids Indole Alkaloids fumigaclavine C Trinitrobenzenesulfonic Acid Matrix Metalloproteinases
Topics	Acremonium (metabolism) Animals Colitis (chemically induced, drug therapy, immunology) Colon (drug effects, metabolism, pathology) Cytokines (genetics, metabolism) Disease Models, Animal Ergot Alkaloids Female Gene Expression Regulation (drug effects) Gene Expression Regulation, Enzymologic (drug effects) Indole Alkaloids (therapeutic use) Inflammation Lymph Nodes (drug effects, metabolism) Matrix Metalloproteinases (genetics, metabolism) Mice Mice, Inbred BALB C Th1 Cells (immunology) Trinitrobenzenesulfonic Acid

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